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Genome-wide mRNA expression analyses of liver cells upon YAP induction (time series Liver_RNAseq_LSL)

ABSTRACT: Genome-wide mRNA expression analyses of liver cells upon YAP induction (time series Liver_RNAseq_LSL)

PROVIDER: PRJNA575011 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10204551_1.fastq.gz	Fastqsanger.gz
	SRR10204551_2.fastq.gz	Fastqsanger.gz
	SRR10204552_1.fastq.gz	Fastqsanger.gz
	SRR10204552_2.fastq.gz	Fastqsanger.gz
	SRR10204553_1.fastq.gz	Fastqsanger.gz

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Genome-wide chromatin analyses of liver cells upon YAP induction [time series Liver_ChIPseq_LSL]

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Genome-wide chromatin analyses of liver cells upon YAP induction [Liver_ChIPSeq_LapTTA]

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Genome-wide chromatin analyses of liver cells upon YAP induction [time series; Liver_ChIPseq_LSL]

Project description:YAP1 is a transcriptional co-activator regulated by the Hippo pathway, mechano-transduction, G-protein coupled receptors and WNT signaling. YAP1 activity depends on its stabilization and its nuclear localization. Once in the nucleus, YAP1 can regulate gene expression by interacting with transcription factors with DNA binding capability. While YAP1 main transcriptional partners belong to the TEAD family, several reports indicate that YAP1 can also associate with SMADs, RUNX and other transcription factors. YAP1 acts as a broad regulator of cell growth and differentiation, thus playing a pivotal role in regeneration, re-programming and cancer. How YAP1 may control such a large number of cellular processes is still to be fully understood. To identify how YAP1 controls transcription and to define gene expression programs directly regulated by YAP1, we conducted a genome wide investigation in the mouse liver. Integrated analyses of ChIP-seq and RNA-seq data indicated that YAP1 can act both as an activator and as a repressor in a context dependent way, and allowed the dissection of transcriptional mechanisms. Longitudinal analysis by ChIP-seq and RNA-seq highlighted differences in genome binding and transcriptional control which allowed the identification of acute and tonic YAP1 dependent responses. While during acute activation YAP1 supported cell cycle and signal transduction programs, its prolonged activation sustained a feedforward loop that potentiated and expanded YAP1 dependent transcription thus leading to the direct engagement of cell identity programs. Overall this study provides a genome scale understanding of how YAP1 controls gene expression and reveals principles in gene regulation which account for YAP1 ability to orchestrate development, regeneration and cell reprogramming.

2022-07-25 | GSE138186 | GEO

Genome-wide mRNA expression analyses of liver cells upon YAP induction (time series; Liver_RNAseq_LSL)

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Analysis of hippo pathway upon YAP knockdown and MEK inhibition

Project description:This experiment analyzes the global proteome and phosphoproteome in YAP amplified cell lines upon YAP knockdown and/or MEK inhibition.

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Transcription profiling of human YAP wild-type or mutants overexpressing MCF10A cells

Project description:This study compares gene expression change upon expression of Yes-associated protein (YAP) wild-type or mutants in order to establish the importance of TEAD binding and WW domains in the gene-induction function of YAP. The results indicate that gene-induction is seriously comprised in YAP-S94A (TEAD binding domain mutant) expressing cells. And mutantion of WW domains (YAP-W1W2) also affect a fraction of YAP induced genes. Therefore both TEAD binding domain and WW domains are required for the full function of YAP in gene-induction. Experiment Overall Design: Four samples are included: 1. pQCXIH vector control; 2 YAP-WT expression; 3. YAP-S94A expression; 4. YAP-W1W2 expression. Gene expression profiles of YAP wild-type or mutants expressing cells were compared to that of vector control. Experiments were done in MCF10A mammary epithelial cells.

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Project description:Transcriptome analysis of prostate cancer patient derived organoid DU145 cell line upon knockdown of YAP, TAZ, or YAP/TAZ mediated by siRNAs

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RNA-Seq of MSK-PCa3 prostate cancer organoids upon knockdown of FOSL1, YAP, TAZ, or YAP/TAZ

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